Intraoperative observations, necropsy, and angiographic studies suppor
t the presumption that neurovascular compression of the left ventrolat
eral medulla may cause neurogenic hypertension. Pulsatile irritation o
f the ventrolateral medulla at the root-entry zone of cranial nerves I
X and X increases blood pressure in animals. To identify and assess th
e distribution of neurovascular compression at the ventrolateral medul
la in human beings, we did a prospective single-blind study in 24 pati
ents with essential hypertension, in 14 patients with renal hypertensi
on, and in 14 normal subjects. To detect neurovascular compression, we
used axial and coronal and magnetic-resonance angiography Blood press
ure control and duration of hypertension were not different in the two
groups of patients. 20 patients with essential hypertension had magne
tic tomographic evidence of left-sided neurovascular compression at th
e ventrolateral medulla; 2 patients with renal hypertension and 1 of t
he normal subjects had a positive finding on the left. On the right si
de, we found signs of neurovascular compression in 4 patients with ess
ential hypertension, in 4 with renal hypertension, and in 2 of the nor
mal subjects. With magnetic resonance tomography, it is possible to ev
aluate the neurovascular relations in the posterior fossa and detect n
eurovascular compression at the ventrolateral medulla. These data in l
iving subjects give further evidence of an association between neurova
scular compression at the left ventrolateral medulla acid essential hy
pertension.